Act1 mediates IL-17–induced EAE pathogenesis selectively in NG2 + glial cells

In this study, the authors show that depletion of the IL-17 signaling component, Act1, specifically from NG2+ glia led to a substantial reduction in the severity of pathology in an EAE mouse model. They also find that IL-17 induces apoptosis of NG2+ cells in an Act1-dependent manner.